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综述了一些癌基因、肿瘤抑制基因和DNA修复基因对细胞电离辐射敏感性的影响。涉及到癌基因在细胞辐射反应中的作用,尤其是那些已被广泛研究的癌基因,如ras基因家族。对于肿瘤抑制基因,主要综述了p53,这是一种被认为能影响辐射敏感性的基因。一般认为细胞周期中有检点因子,并假定它能捕获G_1期受照细胞使之在进入DNA合成期前修复损伤。目前有6种DNA修复基因已在哺乳动物细胞中克隆化,但仅有一种XRCC1涉及到人类细胞X射线损伤修复,当这种基因转入EM_9细胞时,XRCC1能纠正高水平姐妹染色单体互换率,但其表达似乎与人类头颈部肿瘤细胞的辐射敏感性无关。辐射敏感性是一个复杂的问题,它涉及许多因素。给出了一个照射后细胞反应过程的图解,提示电离辐射引发的一系列可能事件。
The effects of some oncogenes, tumor suppressor genes and DNA repair genes on the sensitivity of cell ionizing radiation were reviewed. The role of oncogenes in the cellular radiation response is involved, especially those that have been extensively studied, such as the ras gene family. For tumor suppressor genes, p53 is primarily reviewed, a gene that is believed to influence radiation sensitivity. It is generally believed that there is a checkpoint factor in the cell cycle, and it is assumed that it can capture Gl-phase irradiated cells to repair damage before entering the DNA synthesis phase. At present, six DNA repair genes have been cloned in mammalian cells, but only one XRCC1 is involved in the repair of human cell X-ray damage. When this gene is transferred into EM_9 cells, XRCC1 can correct high-level sister chromatid interactions. Exchange rate, but its expression seems to have nothing to do with the radiation sensitivity of human head and neck tumor cells. Radiation sensitivity is a complex issue that involves many factors. An illustration of the cell reaction process after irradiation is given, suggesting a series of possible events triggered by ionizing radiation.